I. Field of the Invention
This invention relates generally to cardiac rhythm management devices including bradycardia pacemakers, cardioverters and defibrillators, and more particularly to a device in which the heart's Active Time is used as a controlling variable.
II. Discussion of the Prior Art
Beginning in about 1976, a variety of cardiac pacemakers have been developed and disclosed in which a physiologic or a non-physiologic sensor is used to produce a signal which is intended to be proportional to the level of work or exercise being performed by the patient. Specifically, in 1977, Dr. Mario Alcidi, in U.S. Pat. No. 4,009,721, described a system in which blood pH is sensed and a control signal proportional thereto is developed for altering the rate of an implanted pacemaker. That device has not proven to be commercially successful because it is difficult to implement. Stable pH electrodes are not generally available. The measurement is not related directly to exercise level and any feedback of information as to hemodynamic instability is too slow.
The Cook et al. U.S. Pat. No. 4,543,954 describes a system in which blood temperature becomes the rate controlling parameter for an implanted pacemaker. While blood temperature is found to increase during exercise and emotional stress, the main problems in using temperature as a rate controlling parameter are that the response to the onset of exercise is too slow and temperature change is found not to be proportional to the exercise level. Again, no hemodynamic feedback information is provided when this approach is utilized.
The Richards U.S. Pat. No. 4,228,803 disclose the idea of using the QT interval of the electrocardiogram as the rate control parameter. This interval is found to decrease with increases in exercise. While it has been shown useful for some patients, the technique suffers from the problem that the T-wave is difficult to sense and the interval itself changes between sensed and paced beats, providing only relative values. Beta blockage results in inhibition of catecholamine response and therefore reduction of the stimulus-to-T-wave change. The approach also does not provide any hemodynamic feedback relating to the effect of the heart rate change on the circulatory system.
Still another variety of rate adaptive pacemaker incorporates a pressure sensor for detecting blood pressure changes. See U.S. Pat. No. 4,899,752 to Cohen. Such a sensor is used to measure the rate of increase of the intraventricular pressure. Increased pressure gradient is associated with cardiovascular stress through increased circulating catecholamines and the Frank-Starling response. The Frank-Starling law provides that as increases in venous return further distends the ventricle, the myocardiofibers contract with greater force. Circulating catecholamines, such as epinephrine, cause increased contractile force by affecting beta receptors. This increase in the rate of pressure rise is sensed by a pressure transducer in a pacing lead capable of measuring pressure changes. The rate of change in pressure is changed by the dynamics of the contraction. Therefore, intrinsic and paced beats result in different level signals leading to rate changes which are not exercise-related.
The Wirtzfeld U.S. Pat. No. 4,399,820 employs a sensor capable of measuring oxygen saturation of venous blood for developing a rate control signal as a function thereof. Because oxygen saturation of venous blood decreases with increased exercise, low work loads cause a significant decrease in oxygen saturation. Changes are not linearly related to the applied load. Moreover, leads for monitoring oxygen saturation tend to be quite complex and are not $ particularly reliable over a long term. The device does not provide hemodynamic feedback.
The Dahl U.S. Pat. No. 4,140,132, assigned to Medtronics, Inc., describes a rate adaptive pacer which is perhaps the most widely used rate adaptive system. It relies upon motion or activity, but there is a lack of correlation between motion and the actual work load being experienced by the patient. Thus, its popularity is based principally upon its intrinsic simplicity and not its physiologic response.
In the Krasner U.S. Pat. No. 3,593,718, a lead system is provided for measuring impedance changes in the thoracic cavity. When respiration increases, heart rate generally increases, except for periods of voluntary control of respiration, such as during speech. Both impedance respiratory frequency and impedance respiratory tidal volume are parameters that are sensed. This system does not take into account the change in the artery-venous difference of oxygen concentration that increases the oxygen uptake per liter of inspired air. Oxygen uptake also is susceptible to changes in the oxygen concentration of the inspired gas. This approach does not produce any hemodynamic feedback information to the implanted pacemaker.
The foregoing prior art systems with their mentioned sensors are deficient in that they are incapable of providing the patient an adequate heart rate under all conditions because none is looking at the basic hemodynamics of the heart contraction. An optimized pacing system should be capable of determining the optimum heart rate for the patient under all conditions. While nearly all of the prior art systems alluded to above involve sensors whose outputs are monitored to identify features known to occur during exercise, practically no attention has been focused on monitoring hemodynamic parameters that are crucial to circulatory physiology. For instance, it is commonly assumed that an increase in heart rate will produce an increase in cardiac output. This is not always true. The supposition is correct only if the following two conditions are met:
(1) The heart muscle must be in condition to support the increased work load (calcium availability, lack of ischemia, etc.); and PA0 (2) Sufficient blood must be returning to the heart to maintain cardiac output.
In a healthy individual, exercise increases circulating catecholamine, reduces the pre-ejection interval, increases dP/dT max, decreases the ejection time, and decreases -dP/dT max. All of the above changes decrease the time the ventricle is active, i.e., from the pacing spike to the end of the fast filling phase. The changes with exercise are also associated with an increase in heart rate, which, in turn, decreases passive time, i.e., the diastolic phase. At maximum load, the passive time is very small, with only the fast filling phase in evidence. The maximum heart rate is primarily determined by the capacity of the heart to reduce its total Active Time, and the capacity of the venous system to refill the right and left ventricles during the fast filling phase. As used herein, the term "Active Time" (sometimes abbreviated to "AT" ) comprises the total time that would elapse from the ventricular pacing pulse or the ventricular sensed R-wave to the end of the filling phase, provided that the ventricles are refilled at the fast filling rate.